Ventilatory response to exercise in patients with left-to-right shunts.

The progression of chronic obstructive pulmonary disease (COPD) is generally associated with decreased exercise capacity. Differences in forced expired volume in 1 s (FEV1) among patients account for only a fraction of the variability in maximal oxygen consumption (VO2max). We hypothesized that variability in ventilatory response to exercise and in inspiratory mechanics and body mass index contributes importantly to variability in VO2max in this disease. We analyzed the files of 53 patients with established diagnosis of COPD who underwent a recent symptom-limited exercise test. We used inspiratory capacity and maximum inspiratory flow as measures of variability in inspiratory mechanics. The minute ventilation (VE) at the subject's VO2max was divided by the predicted in a normal subject at the same VO2 to obtain a ratio (VE,max/VE,pred). The ventilatory response during exercise provided the best correlation with peak VO2 (r = 0.62). FEV1 and inspiratory capacity also correlated with peak oxygen consumption but not as well as the ventilatory response (r = 0.49 and r = 0.46, respectively). Maximum inspiratory flow and body mass index showed only weak positive correlations (r = 0.23, not significant). The stepwise analysis generated the following equation: VO2max (%predicted) = (77.26 x VE,pred/VE,max) + [0.45 x FEV1 (%predicted)] - 23.66; r = 0.76, P < 0.001. We conclude that variability in the ventilatory response during exercise is one of the main determinants of variability in exercise capacity in COPD patients.

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Neuro-hormonal activation predicts ventilatory response to exercise and functional capacity in patients with heart failure

European Journal of Heart Failure ◽

10.1016/j.ejheart.2005.05.007 ◽

2005 ◽

Vol 8 (1) ◽

pp. 46-53 ◽

Cited By ~ 31

Author(s):

Claudio Passino ◽

Roberta Poletti ◽

Francesca Bramanti ◽

Concetta Prontera ◽

Aldo Clerico ◽

...

Keyword(s):

Heart Failure ◽

Functional Capacity ◽

Ventilatory Response ◽

Patients With Heart Failure ◽

Hormonal Activation ◽

Response To Exercise

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Ventilatory Response to Exercise after Intracardiac Repair of Tetralogy of Fallot

American Review of Respiratory Disease ◽

10.1164/ajrccm/144.4.833 ◽

1991 ◽

Vol 144 (4) ◽

pp. 833-836 ◽

Cited By ~ 14

Author(s):

Geordie P. Grant ◽

Robert P. Garofano ◽

Anthony L. Mansell ◽

Harris B. Leopold ◽

Welton M. Gersony

Keyword(s):

Tetralogy Of Fallot ◽

Ventilatory Response ◽

Intracardiac Repair ◽

Response To Exercise

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Influence of Locomotor Muscle Metaboreceptor Stimulation on the Ventilatory Response to Exercise in Heart Failure

Circulation Heart Failure ◽

10.1161/circheartfailure.109.879684 ◽

2010 ◽

Vol 3 (2) ◽

pp. 212-219 ◽

Cited By ~ 40

Author(s):

Thomas P. Olson ◽

Michael J. Joyner ◽

Bruce D. Johnson

Keyword(s):

Heart Failure ◽

Ventilatory Response ◽

Response To Exercise

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Effect of mild hypoxia on ventilation during exercise

Journal of Applied Physiology ◽

10.1152/jappl.1962.17.2.239 ◽

1962 ◽

Vol 17 (2) ◽

pp. 239-242 ◽

Cited By ~ 12

Author(s):

Thomas F. Hornbein ◽

Albert Roos

Keyword(s):

Steady State ◽

Ventilatory Response ◽

Human Subjects ◽

Sympathetic Innervation ◽

Mild Degree ◽

Flow Through ◽

Neural Discharge ◽

Response To Exercise ◽

Mild Hypoxia ◽

Rest And Exercise

Hypoxia of mild degree (PaOO2 above 60 mm Hg) produces little or no ventilatory response in resting man during the steady state. To evaluate the possibility that the effectiveness of a hypoxic chemoreceptor drive might be enhanced by exercise, the ventilatory response to mild hypoxia was measured in two human subjects during rest and exercise. Though no significant increase in ventilation occurred at rest above a PaOO2 of 60 mm Hg, a decrease in PaOO2from 100 to 94 mm Hg produced a statistically significant increase in steady state ventilation during moderate exercise. In addition, temporary block of the sympathetic innervation to the carotid and aortic bodies in one subject resulted in a diminution of work hyperpnea. This suggests that increased sympathetic tone during exercise, by reducing blood flow through the chemoreceptors, might result in increased neural discharge and hence increased ventilation even though arterial POO2 is the same as at rest. Thus, activity of the chemoreceptors as modified by sympathetic control of their blood supply may be an important determinant of the ventilatory response to exercise. Since work hyperpnea is enhanced by even mild hypoxia, this ventilatory response may be sufficient to initiate respiratory acclimatization to altitudes so low that resting ventilation on acute exposure is unaffected. Submitted on July 31, 1961

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Ventilatory response to exercise in subjects breathing CO2 or HeO2

Journal of Applied Physiology ◽

10.1152/jappl.1997.82.3.746 ◽

1997 ◽

Vol 82 (3) ◽

pp. 746-754 ◽

Cited By ~ 65

Author(s):

T. G. Babb

Keyword(s):

Maximal Exercise ◽

Respiratory Mechanics ◽

Ventilatory Threshold ◽

Ventilatory Response ◽

Minute Ventilation ◽

Normal Lung ◽

Normal Lung Function ◽

Older Subjects ◽

Breathing Room ◽

Response To Exercise

Babb, T. G. Ventilatory response to exercise in subjects breathing CO2 or HeO2. J. Appl. Physiol. 82(3): 746–754, 1997.—To investigate the effects of mechanical ventilatory limitation on the ventilatory response to exercise, eight older subjects with normal lung function were studied. Each subject performed graded cycle ergometry to exhaustion once while breathing room air; once while breathing 3% CO2-21% O2-balance N2; and once while breathing HeO2 (79% He and 21% O2). Minute ventilation (V˙e) and respiratory mechanics were measured continuously during each 1-min increment in work rate (10 or 20 W). Data were analyzed at rest, at ventilatory threshold (VTh), and at maximal exercise. When the subjects were breathing 3% CO2, there was an increase ( P < 0.001) inV˙e at rest and at VTh but not during maximal exercise. When the subjects were breathing HeO2,V˙e was increased ( P < 0.05) only during maximal exercise (24 ± 11%). The ventilatory response to exercise below VTh was greater only when the subjects were breathing 3% CO2( P < 0.05). Above VTh, the ventilatory response when the subjects were breathing HeO2 was greater than when breathing 3% CO2( P < 0.01). Flow limitation, as percent of tidal volume, during maximal exercise was greater ( P < 0.01) when the subjects were breathing CO2 (22 ± 12%) than when breathing room air (12 ± 9%) or when breathing HeO2 (10 ± 7%) ( n = 7). End-expiratory lung volume during maximal exercise was lower when the subjects were breathing HeO2 than when breathing room air or when breathing CO2( P < 0.01). These data indicate that older subjects have little reserve for accommodating an increase in ventilatory demand and suggest that mechanical ventilatory constraints influence both the magnitude of V˙eduring maximal exercise and the regulation ofV˙e and respiratory mechanics during heavy-to-maximal exercise.

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Control of breathing at the start of exercise as influenced by posture

Journal of Applied Physiology ◽

10.1152/jappl.1983.55.5.1460 ◽

1983 ◽

Vol 55 (5) ◽

pp. 1460-1466 ◽

Cited By ~ 34

Author(s):

D. Weiler-Ravell ◽

D. M. Cooper ◽

B. J. Whipp ◽

K. Wasserman

Keyword(s):

Stroke Volume ◽

Phase I ◽

Ventilatory Response ◽

Normal Subjects ◽

Initial Increase ◽

Base Line ◽

Co2 Output ◽

End Tidal ◽

Response To Exercise ◽

Initial Change

It has been suggested that the initial phase of the ventilatory response to exercise is governed by a mechanism which responds to the increase in pulmonary blood flow (Q)--cardiodynamic hyperpnea. Because the initial change in stroke volume and Q is less in the supine (S) than in the upright (U) position at the start of exercise, we hypothesized that the increase in ventilation would also be less in the first 20 s (phase I) of S exercise. Ten normal subjects performed cycle ergometry in the U and S positions. Inspired ventilation (VI), O2 uptake (VO2), CO2 output (VCO2), corrected for changes in lung gas stores, and end-tidal O2 and CO2 tensions were measured breath by breath. Heart rate (HR) was determined beat by beat. The phase I ventilatory response was markedly different in the two positions. In the U position, VI increased abruptly by 81 +/- 8% (mean +/- SE) above base line. In the S position, the phase I response was significantly attenuated (P less than 0.001), the increase in VI being 50 +/- 6%. Similarly, the phase I VO2 and VO2/HR responses reflecting the initial increase in Q and stroke volume, were attenuated (P less than 0.001) in the S posture, compared with that for U; VO2 increased 49 +/- 5.3 and 113 +/- 14.7% in S and U, respectively, and VO2/HR increased 16 +/- 3.0 and 76 +/- 7.1% in the S and U, respectively. The increase in VI correlated well with the increase in VO2, (r = 0.80, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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